This research is designed to elucidate cellular, neuronal, and mechanical factors that are important determinants in vascular control of peripheral resistance during the development and maintenance of hypertension, and as a result of antihypertensive treatment. The study focusses on in vitro measurements of viable 75-200 micrometer arteries from the mesenteric, cerebral and coronary vascular beds of the spontaneously hypertensive rat (SHR) and the normotensive Wistar/Kyoto rat (WKY). Answers to the following questions will be sought: 1) During hypertension development, are contractile proteins altered in any other way than in proportion to hyperplasia, and do the temporal dynamics of cell and wall parameters suggest a pressure-dependent cause? 2) During the maintenance of hypertension, are the greater vessel contractures a consequence of hyperplasia and more contractile material, or are the protein and cellular characteristics modified? Are the nerve-muscle cleft widths and innervation density changed? Is myogenic propagation altered as a result of modified cellular connections or membrane properties? 3) What are the effects of Captopril, Prazosin, and combined hydralazine/reserpine/hydrochlorothiazide treatments on vessel morphology and chemistry, and contractility? 4) Do all of these changes occur uniformly in the 3 beds. Specific measrements will be made of: cell division rates using autoradioautography; actin:myosin using micro-gel electrophoresis, micro-protein and nanogram DNA techniques; collagen synthesis; contractile mechanics and excitation-contraction-coupling using miniaturized myographs, microelectrodes and video microscopic recordings. The correlative nature of the multiple measures proposed on the vessels of a single bed, and between beds in a single animal, will comprise a matrix of new information. This study will therefore provide a valuable contribution to the understanding of small artery involvement in the etiology, maintenance and treatment of hypertension.